28 results on '"Masato Yozu"'
Search Results
2. Untutored learning curve for endoscopic submucosal dissection in New Zealand.
- Author
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Fox, Tara, Masato Yozu, Sze-Lin Peng, Schauer, Cameron, and Sekra, Anurag
- Published
- 2024
- Full Text
- View/download PDF
3. Non‐conventional dysplasia is frequently associated with low‐grade tubuloglandular and mucinous adenocarcinomas in inflammatory bowel disease
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Fahire Goknur Akarca, Masato Yozu, Lindsay Alpert, Bence P Kővári, Lei Zhao, Marcela Salomao, Xiaoyan Liao, Maria Westerhoff, Gregory Y Lauwers, and Won‐Tak Choi
- Subjects
Histology ,General Medicine ,Pathology and Forensic Medicine - Published
- 2023
4. Non‐conventional dysplasias of the tubular gut: a review and illustration of their histomorphological spectrum
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Rish K. Pai, Tetsuo Ushiku, Kun Jiang, Won-Tak Choi, Ian Brown, Yukihiro Nakanishi, Baek Hyun Kim, Paula Chaves, Gregory Y. Lauwers, Ryoji Kushima, Till Clauditz, Kyoung Mee Kim, Bence Kővári, Daniela Pereira, Masato Yozu, Gregory Miller, John R. Goldblum, Amitabh Srivastava, Masoumeh Ghayouri, and Marian Priyanthi Kumarasinghe
- Subjects
Gastritis, Atrophic ,0301 basic medicine ,medicine.medical_specialty ,Histology ,Colon ,Duodenum ,Gastrointestinal Diseases ,Atrophic gastritis ,Inflammatory bowel disease ,Gastroenterology ,Endoscopy, Gastrointestinal ,Pathology and Forensic Medicine ,Diagnosis, Differential ,Barrett Esophagus ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Gastrointestinal tract ,business.industry ,General Medicine ,Inflammatory Bowel Diseases ,medicine.disease ,Gastrointestinal Microbiome ,Gastrointestinal Tract ,030104 developmental biology ,medicine.anatomical_structure ,Dysplasia ,030220 oncology & carcinogenesis ,Practice Guidelines as Topic ,business ,Precancerous Conditions - Abstract
The increasing use of gastrointestinal endoscopic procedures has led to the recognition by histopathologists of non-conventional (or special-type) dysplasias of the gastrointestinal tract. These lesions can be recognised in association with prevalent underlying gastrointestinal conditions, such as Barrett oesophagus, chronic atrophic gastritis, and inflammatory bowel disease. The diagnosis of these special types can be challenging, and their biological behaviours are not fully characterised. The aim of this review is to provide a global view of non-conventional dysplastic lesions observed in the various segments of the tubular gastrointestinal tract and describe their salient features. Furthermore, as the clinical implications of these various subtypes have not been broadly tested in practice and are not represented in most management guidelines, we offer guidance on the best management practices for these lesions.
- Published
- 2021
5. Gastrointestinal stromal tumour (GIST) arising in Meckel’s diverticulum
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Ak Muhd Izzan Zulfiqah, Linda Leys, and Masato Yozu
- Subjects
Pathology and Forensic Medicine - Published
- 2022
6. Australasian Gastrointestinal Pathology Society (AGPS) consensus guidelines for universal defective mismatch repair testing in colorectal carcinoma
- Author
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Ian Brown, Anthony J. Gill, Christophe Rosty, M. Priyanthi Kumarasinghe, and Masato Yozu
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0301 basic medicine ,congenital, hereditary, and neonatal diseases and abnormalities ,medicine.medical_specialty ,Cost effectiveness ,MLH1 ,DNA Mismatch Repair ,Pathology and Forensic Medicine ,03 medical and health sciences ,0302 clinical medicine ,Neoplastic Syndromes, Hereditary ,Humans ,Medicine ,Intensive care medicine ,neoplasms ,Early Detection of Cancer ,Brain Neoplasms ,business.industry ,Endometrial cancer ,Australia ,nutritional and metabolic diseases ,Microsatellite instability ,Gastrointestinal pathology ,Mismatch Repair Protein ,medicine.disease ,digestive system diseases ,Lynch syndrome ,030104 developmental biology ,030220 oncology & carcinogenesis ,Mutation ,Microsatellite Instability ,DNA mismatch repair ,Colorectal Neoplasms ,business ,New Zealand - Abstract
Lynch syndrome is the most common hereditary form of colorectal carcinoma caused by a constitutional pathogenic mutation in a DNA mismatch repair gene. Identifying Lynch syndrome is essential to initiate intensive surveillance program for the patient and affected relatives. On behalf of the Australasian Gastrointestinal Pathology Society (AGPS), we present in this manuscript consensus guidelines for Lynch syndrome screening in patients with colorectal carcinoma. The goal of this consensus document is to provide recommendations to pathologists for diagnosis of Lynch syndrome with discussion of the benefits and limitations of each test. Universal screening for defective mismatch repair is recommended, in agreement with the recent endorsement of universal testing by the National Health and Medical Research Council in Australia and the New Zealand Ministry of Health. The value of evaluating defective mismatch repair is acknowledged not only for Lynch syndrome screening but also for therapeutic decision information in patient management. AGPS advocates appropriate government funding for the molecular tests necessary for Lynch syndrome screening (BRAF mutation, MLH1 methylation testing).
- Published
- 2019
7. Histologic and Outcome Study Supports Reclassifying Appendiceal Goblet Cell Carcinoids as Goblet Cell Adenocarcinomas, and Grading and Staging Similarly to Colonic Adenocarcinomas
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Michelle Yang, Gregory Y. Lauwers, Namrata Setia, David P. Ryan, Masato Yozu, Melanie Johncilla, Robert D. Odze, James C. Cusack, Leona A. Doyle, Joseph Misdraji, and Amitabh Srivastava
- Subjects
Adult ,Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,Biopsy ,Carcinoid Tumor ,Adenocarcinoma ,Pathology and Forensic Medicine ,03 medical and health sciences ,0302 clinical medicine ,Predictive Value of Tests ,Terminology as Topic ,Humans ,Medicine ,Stage (cooking) ,Grading (tumors) ,Goblet cell carcinoid ,Aged ,Neoplasm Staging ,Aged, 80 and over ,Neoplasm Grading ,Goblet cell ,medicine.diagnostic_test ,business.industry ,Mucin ,Middle Aged ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,Appendiceal Neoplasms ,030220 oncology & carcinogenesis ,Colonic Neoplasms ,Female ,Surgery ,Goblet Cells ,Anatomy ,business - Abstract
Goblet cell carcinoid tumors are amphicrine tumors whose biological behavior ranges from indolent to highly aggressive, depending on tumor grade. Current grading systems for these tumors are based on identifying an adenocarcinoma arising in the setting of a goblet cell carcinoid tumor, which distinguishes this tumor from other gastrointestinal tract adenocarcinomas. Because goblet cell tumors are predominantly tumors of mucin secreting cells, we propose that they be classified as goblet cell adenocarcinomas, and graded using a methodology that has parallels in colorectal adenocarcinoma grading. We graded a large series of goblet cell adenocarcinomas by assessing the proportion of the tumor that demonstrates tubular or clustered growth. Histologic grade correlated with overall survival independent of stage, with median overall survival of 204, 86, and 29 months for low-grade, intermediate-grade, and high-grade goblet cell adenocarcinomas, respectively. Tumor stage also correlated with overall survival. We also graded the tumors according to previously proposed grading systems, and found that these systems are valid, in that they segregate patients according to prognosis.
- Published
- 2018
8. Mutational landscape of goblet cell carcinoids and adenocarcinoma ex goblet cell carcinoids of the appendix is distinct from typical carcinoids and colorectal adenocarcinomas
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Gregory Y. Lauwers, Melanie Johncilla, Joseph Misdraji, Neal I. Lindeman, Robert D. Odze, Masato Yozu, Mikhail Lisovsky, Amitabh Srivastava, and Matthew D. Stachler
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Adult ,Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,ARID1A ,Carcinoid Tumor ,Adenocarcinoma ,Biology ,medicine.disease_cause ,Pathology and Forensic Medicine ,CDH1 ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Humans ,neoplasms ,Exome sequencing ,Goblet cell carcinoid ,Aged ,Goblet cell ,Middle Aged ,medicine.disease ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,medicine.anatomical_structure ,Appendiceal Neoplasms ,030220 oncology & carcinogenesis ,Mutation ,biology.protein ,Female ,CDKN1B ,KRAS ,Colorectal Neoplasms - Abstract
There is limited data on the spectrum of molecular alterations in goblet cell carcinoids and adenocarcinoma ex goblet cell carcinoids of the appendix. We used next generation sequencing to determine mutations of potential pathogenetic and therapeutic significance in this rare group of tumors. Adequate DNA was successfully extracted in 34/46 cases and the final group included 18 goblet cell carcinoids and 16 adenocarcinoma ex goblet cell carcinoids. Illumina TruSeq™ was used for sequencing exons of a custom 282 gene panel using an Illumina HiSeq 2000. All cases had a minimum coverage depth of at least 50 reads. After filtering through the Exome Sequencing Project, the number of mutations per case ranged from 0–9 (mean:3). The mutational burden in adenocarcinoma ex goblet cell carcinoids was significantly higher than goblet cell carcinoids (mean 5 vs. 3; p
- Published
- 2018
9. Gastric pyloric gland adenoma: a multicentre clinicopathological study of 67 cases
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Ian Brown, Namrata Setia, Tetsuo Ushiku, Gregory Y. Lauwers, Amitabh Srivastava, Masato Yozu, Won-Tak Choi, Joseph Misdraji, Rish K. Pai, Ryan M. Gill, Masashi Fukayama, and Melanie Johncilla
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Adenoma ,Adult ,Male ,0301 basic medicine ,medicine.medical_specialty ,Histology ,Autoimmune Gastritis ,Adenocarcinoma ,Gastroenterology ,Pathology and Forensic Medicine ,Familial adenomatous polyposis ,Young Adult ,03 medical and health sciences ,0302 clinical medicine ,Immunophenotyping ,Stomach Neoplasms ,Internal medicine ,Biomarkers, Tumor ,medicine ,Genetic predisposition ,Humans ,Aged ,Aged, 80 and over ,business.industry ,General Medicine ,Middle Aged ,medicine.disease ,Cell Transformation, Neoplastic ,030104 developmental biology ,Gastric Mucosa ,Dysplasia ,030220 oncology & carcinogenesis ,Disease Progression ,Immunohistochemistry ,Female ,Neoplasm Recurrence, Local ,business - Abstract
AIMS There is limited information regarding the clinicopathological and immunohistochemical characteristics of gastric pyloric gland adenomas (PGAs). METHODS AND RESULTS Sixty-seven cases of gastric PGA from 57 patients were analysed. PGAs occurred with similar frequency in men and women (47.4 and 52.6%, respectively), with a mean age of 66 years. Most presented in the gastric body/fundus (67.2%). Fifteen cases (22.4%) developed against a background of autoimmune gastritis (AIG), whereas normal mucosa was seen in 35.8%. Only 16.4% (11 cases) developed in patients with a genetic predisposition, most commonly familial adenomatous polyposis. Low-grade lesions had a mean size of 1.5 cm, while PGAs with high-grade dysplasia (HGD) or adenocarcinoma had a mean size of 3.5 cm (P < 0.001) and more commonly showed tubulovillous architecture (50.0 versus 25.6% in low-grade dysplasia; P = 0.040). Most PGAs (61.2%) co-expressed mucin (MUC)5AC and MUC6 (mixed type), which was associated significantly with HGD or adenocarcinoma (P = 0.013). AIG was also associated with HGD (P = 0.027), but genetic predisposition did not correlate with the grade of dysplasia (P = 0.793). The recurrence rate of PGA was similar for high- (11.8%) and low-grade lesions (7.4%) (P = 0.624). CONCLUSIONS The risk of HGD increases with the size of PGA, tubulovillous architecture and the presence of AIG as well as mixed immunophenotype. As the overall local recurrence rate is less than 10%, PGAs may be treated conservatively, but they should be excised completely if possible, particularly if they are large or show high-grade features.
- Published
- 2018
10. Nonconventional dysplasia in patients with inflammatory bowel disease and colorectal carcinoma: a multicenter clinicopathologic study
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Gregory Y. Lauwers, Masato Yozu, Won-Tak Choi, Joseph Misdraji, Priyanthi Kumarasinghe, Gregory Miller, Noam Harpaz, and Angela R. Shih
- Subjects
0301 basic medicine ,Adult ,Male ,Pathology ,medicine.medical_specialty ,Colorectal cancer ,Mixed type ,Gastroenterology ,Inflammatory bowel disease ,Pathology and Forensic Medicine ,Lesion ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,In patient ,Aged ,Retrospective Studies ,Aged, 80 and over ,business.industry ,Not Otherwise Specified ,Retrospective cohort study ,Middle Aged ,medicine.disease ,Inflammatory Bowel Diseases ,digestive system diseases ,030104 developmental biology ,Dysplasia ,030220 oncology & carcinogenesis ,Female ,medicine.symptom ,business ,Colorectal Neoplasms - Abstract
Several types of nonconventional dysplasia have been recently described in inflammatory bowel disease (IBD). However, strict morphologic criteria are lacking, and their clinicopathologic features (including potential association with conventional dysplasia and/or colorectal cancer [CRC]) are poorly understood. A total of 106 dysplastic or serrated lesions in 58 IBD patients with CRC were retrospectively identified from five institutions. Thirty-six cases of nonconventional dysplasia were identified in 26 (45%) of the 58 patients and occurred with similar frequency in men and women (58% and 42%, respectively), with a mean age of 54 years (range: 24–73) and a long history of IBD (mean: 17 years, range: 2–43). Six morphologic patterns were recognized. Hypermucinous dysplasia (n = 15; 42%) presented as either a ‘pure type’ (n = 5; 14%) or a ‘mixed type’ with either conventional or another nonconventional subtype (n = 10; 28%). Serrated lesions, as a group, were equally common (n = 15; 42%) and included three variants: traditional serrated adenoma-like (n = 10; 28%), sessile serrated lesion-like (n = 1; 3%), and serrated lesion, not otherwise specified (n = 4; 11%). Dysplastic lesions with increased Paneth cell differentiation (n = 4; 11%) and goblet cell deficient dysplasia (n = 2; 6%) were rare. Twelve (46%) of the 26 patients had only nonconventional dysplasia, whereas the remaining 14 patients (54%) had both nonconventional and conventional dysplasias. Nonconventional dysplasia was most often graded as low-grade dysplasia (81%), which was less common in conventional dysplasia (37%) (p = 0.003). When present alone, nonconventional dysplasia was predominantly found in the left colon (81%, p = 0.006) as a polypoid or raised lesion (75%, p
- Published
- 2019
11. Loss of expression of MLH1 in non-dysplastic crypts is a harbinger of neoplastic progression in sessile serrated adenomas/polyps
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Marina Kem, Mari Mino-Kenudson, Robert D. Odze, Joseph Misdraji, Masato Yozu, and Odise Cenaj
- Subjects
0301 basic medicine ,Adult ,Male ,congenital, hereditary, and neonatal diseases and abnormalities ,Pathology ,medicine.medical_specialty ,Histology ,Colonic Polyps ,Adenocarcinoma ,MLH1 ,digestive system ,Pathology and Forensic Medicine ,03 medical and health sciences ,Adenomatous Polyps ,Young Adult ,0302 clinical medicine ,Neoplastic progression ,Carcinoma ,Biomarkers, Tumor ,Medicine ,Humans ,neoplasms ,Aged ,Aged, 80 and over ,business.industry ,Serrated polyp ,nutritional and metabolic diseases ,General Medicine ,Middle Aged ,medicine.disease ,digestive system diseases ,030104 developmental biology ,Cell Transformation, Neoplastic ,Dysplasia ,030220 oncology & carcinogenesis ,Colonic Neoplasms ,Disease Progression ,Biomarker (medicine) ,Immunohistochemistry ,Female ,business ,MutL Protein Homolog 1 - Abstract
AIMS Dysplasia in colonic sessile serrated adenomas (SSAs)/sessile serrated polyps often shows loss of MLH1 expression as determined with immunohistochemistry, but the significance of loss of MLH1 expression in non-dysplastic crypts in these polyps is less well studied. The purpose of this study was to evaluate the prevalence of loss of MLH1 expression in non-dysplastic crypts in SSAs, and to evaluate its significance with regard to progression of these polyps. METHODS AND RESULTS Four hundred SSAs, including 158 SSAs without dysplasia, 219 SSAs with dysplasia (SSAD), and 23 SSAs with invasive adenocarcinoma (SSAC), were evaluated immunohistochemically for loss of MLH1 expression in both non-dysplastic and dysplastic portions of the polyps. Seventy-one of 400 (18%) SSAs showed loss of MLH1 expression in non-dysplastic crypts. The prevalence of MLH1-deficient non-dysplastic crypts was higher in polyps with dysplasia or carcinoma (7%, 22%, and 52% in SSAs, SSADs, and SSACs, respectively; P
- Published
- 2019
12. Dabigatran-induced oesophagitis dissecans superficialis
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Masato Yozu and Suneeth Mathew
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medicine.medical_specialty ,business.industry ,Internal medicine ,medicine ,business ,Gastroenterology ,Pathology and Forensic Medicine ,Dabigatran ,medicine.drug - Published
- 2020
13. Essential Components of Melanoma Histopathological Reporting: The Surgical Oncologist’s Perspective
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Jon A. Mathy, Vinka Nurdjaja, and Masato Yozu
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Surgical oncologist ,medicine.medical_specialty ,business.industry ,Melanoma ,Perspective (graphical) ,Cancer ,Dermatology ,Review Article ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,lcsh:RC254-282 ,03 medical and health sciences ,0302 clinical medicine ,Oncology ,030220 oncology & carcinogenesis ,Cutaneous melanoma ,medicine ,Clinical significance ,030212 general & internal medicine ,Radiation treatment planning ,Intensive care medicine ,business - Abstract
Histopathological reporting plays a critical role in guiding the surgical oncologist’s management plan in treatment of primary cutaneous melanoma. The International Collaboration on Cancer Reporting (ICCR) espouses various components of structured histopathological reporting as “essential” or “recommended.” From a surgical oncologist’s perspective, we discuss the clinical relevance of each essential component, as well as prognostic and treatment implications with regard to treatment planning.
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- 2018
14. Heterotopic skin in meckel’s diverticulum – a case report
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Masato Yozu and Se Mi Kim
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Meckel's diverticulum ,business.industry ,Medicine ,Anatomy ,business ,medicine.disease ,Pathology and Forensic Medicine - Published
- 2019
15. Recurrent loss of heterozygosity correlates with clinical outcome in pancreatic neuroendocrine cancer
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Michael Findlay, Ben Lawrence, Braden Woodhouse, Esther Coats, Papaarangi Reid, Mik Black, Masato Yozu, Kimiora Henare, Richard Babor, Jonathan Koea, Sean M. Grimmond, Nicole Kramer, Nicholas Knowlton, Kate Parker, Saxon Connor, Paula Shields, Dragan Damianovich, Cherie Blenkiron, Peter Johnston, Andrew D. MacCormick, Vicky Fan, Marianne S. Elston, Helen Morrin, Peter Tsai, Bridget A. Robinson, Richard W. Carroll, Christopher Jackson, Sandra Fitzgerald, Patrick Yap, Nooriyah Poonawala, Tamsin Robb, Cristin G. Print, Mee Ling Yeong, Sarah M James, Reena Ramsaroop, John A. Windsor, and Adam Bartlett
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0301 basic medicine ,lcsh:QH426-470 ,lcsh:Medicine ,Aneuploidy ,Neuroendocrine tumors ,Gene mutation ,medicine.disease_cause ,Bioinformatics ,Article ,Loss of heterozygosity ,03 medical and health sciences ,0302 clinical medicine ,Pancreatic cancer ,Genetics ,medicine ,PTEN ,MEN1 ,Folliculin ,Molecular Biology ,Genetics (clinical) ,Mutation ,biology ,lcsh:R ,medicine.disease ,lcsh:Genetics ,030104 developmental biology ,030220 oncology & carcinogenesis ,DNA methylation ,Cancer research ,biology.protein - Abstract
Pancreatic neuroendocrine tumors (pNETs) are uncommon cancers arising from pancreatic islet cells. Here we report the analysis of gene mutation, copy number, and RNA expression of 57 sporadic well-differentiated pNETs. pNET genomes are dominated by aneuploidy, leading to concordant changes in RNA expression at the level of whole chromosomes and chromosome segments. We observed two distinct patterns of somatic pNET aneuploidy that are associated with tumor pathology and patient prognosis. Approximately 26% of the patients in this series had pNETs with genomes characterized by recurrent loss of heterozygosity (LoH) of 10 specific chromosomes, accompanied by bi-allelic MEN1 inactivation and generally poor clinical outcome. Another ~40% of patients had pNETs that lacked this recurrent LoH pattern but had chromosome 11 LoH, bi-allelic MEN1 inactivation, and universally good clinical outcome. The somatic aneuploidy allowed pathogenic germline variants (e.g., ATM) to be expressed unopposed, with RNA expression patterns showing inactivation of downstream tumor suppressor pathways. No prognostic associations were found with tumor morphology, single gene mutation, or expression of RNAs reflecting the activity of immune, differentiation, proliferative or tumor suppressor pathways. In pNETs, single gene mutations appear to be less important than aneuploidy, with MEN1 the only statistically significant recurrently mutated driver gene. In addition, only one pNET in the series had clearly actionable single nucleotide variants (SNVs) (in PTEN and FLCN) confirmed by corroborating RNA expression changes. The two clinically relevant patterns of LoH described here define a novel oncogenic mechanism and a plausible route to genomic precision oncology for this tumor type., Cancer: Frequent chromosome loss in rare pancreatic tumors The loss of entire chromosomes seems to be a fundamental driver of tumors arising from the hormone-producing cells of the pancreas. A team led by Cristin Print and Ben Lawrence from the University of Auckland, New Zealand, performed genomic and pathological analysis of 57 pancreatic neuroendocrine tumors, a rare form of cancer caused by the abnormal growth of hormone-producing islet cells within the pancreas. The researchers observed two distinct patterns of chromosome loss, with 26% of the samples missing one copy of 10 specific chromosomes and another 40% lacking a copy of chromosome 11. In both groups, the abnormal chromosome count prompts abnormal gene activity patterns, with recessive mutations unleashed and expressed unopposed. Single gene mutations seem to play only a minor role, suggesting that single gene-targeted drugs will provide little benefit in this disease setting, with more nuanced approaches required.
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- 2017
- Full Text
- View/download PDF
16. Tumour Mutation Profiling with High-throughput Multiplexed Genotyping: A Review of its Use for Guiding Targeted Cancer Therapy
- Author
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Phillip Shepherd, Mark J. McKeage, Donald R. Love, and Masato Yozu
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Cancer Research ,Mutation profiling ,Oncology ,Cancer therapy ,Molecular Medicine ,Computational biology ,Biology ,Bioinformatics ,Throughput (business) ,Genotyping - Published
- 2014
17. Osteoclast-rich undifferentiated carcinoma of the bladder: A case report
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Sinead McCarthy and Masato Yozu
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medicine.anatomical_structure ,Osteoclast ,business.industry ,medicine ,Cancer research ,Undifferentiated carcinoma ,business ,Pathology and Forensic Medicine - Published
- 2018
18. Biphasic gastric adeno-choriocarcinoma in a patient with known lynch syndrome – A case report
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Masato Yozu and Linda Leys
- Subjects
medicine.medical_specialty ,business.industry ,Internal medicine ,Choriocarcinoma ,medicine ,medicine.disease ,business ,Gastroenterology ,Lynch syndrome ,Pathology and Forensic Medicine - Published
- 2018
19. Gastric heterotopia-like duodenal polyps containing Brunner glands with abundant paneth cells and oxyntic cells are frequently associated with advanced left-sided colorectal polyps
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Masato Yozu and Jacklyn Ting
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Gastric heterotopia ,Pathology ,medicine.medical_specialty ,business.industry ,Medicine ,Brunner Glands ,business ,Left sided ,Duodenal polyps ,Pathology and Forensic Medicine - Published
- 2018
20. COUP-TFII Is Preferentially Expressed in the Caudal Ganglionic Eminence and Is Involved in the Caudal Migratory Stream
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Shigeaki Kanatani, Masato Yozu, Kazunori Nakajima, and Hidenori Tabata
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Cerebral Cortex ,Mice, Inbred ICR ,Ganglionic eminence ,General Neuroscience ,Hippocampus ,Cell migration ,Articles ,Biology ,Immunohistochemistry ,Embryonic stem cell ,COUP Transcription Factor II ,Transplantation ,Mice ,medicine.anatomical_structure ,Cell Movement ,Interneurons ,Cerebral cortex ,Cortex (anatomy) ,medicine ,Animals ,Brain Tissue Transplantation ,Calretinin ,Neuroscience ,In Situ Hybridization ,Body Patterning - Abstract
While the cortical interneurons derived from the medial ganglionic eminence (MGE) migrate rather diffusely into the cortex, interneurons that migrate out from the caudal ganglionic eminence (CGE) mainly move caudally into the caudal cerebral cortex and the hippocampus in the form of the caudal migratory stream (CMS) (Yozu et al., 2005). Although transplantation experiments at embryonic day 13.5 had revealed that the migrating cells in these two populations are already intrinsically different in regard to their ability to respond to the CGE environment (Yozu et al., 2005), it is not known how the CGE cells are specified and how their migratory behavior is determined.In this study we showed that, although CGE and lateral ganglionic eminence (LGE) express almost the same marker molecules, LGE cells do not migrate caudally when transplanted into the CGE, suggesting that LGE cells are intrinsically different from CGE cells. We therefore compared the transcriptomes of the CGE, MGE, and LGE, and the results showed thatCOUP-TFIIwas expressed preferentially in the CGE as well as in the migrating interneurons in the CMS. Transplantation experiments revealed that COUP-TFII is sufficient to change the direction of MGE cell migration to caudal when transplanted into the CGE environment, and knockdown ofCOUP-TFIIinhibited the caudal migration of the CGE cells. These results suggest that COUP-TFII is both required and sufficient for the CGE-cell-specific migratory behavior in the caudal direction. Thus, a locally expressed transcription factor determines the migratory direction of the cortical interneurons in a region-specific manner.
- Published
- 2008
21. The Caudal Migratory Stream: A Novel Migratory Stream of Interneurons Derived from the Caudal Ganglionic Eminence in the Developing Mouse Forebrain
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Hidenori Tabata, Masato Yozu, and Kazunori Nakajima
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Telencephalon ,Calbindins ,Transplantation, Heterotopic ,Ganglionic eminence ,Development/Plasticity/Repair ,Population ,Hippocampus ,Biology ,Interneuron migration ,Mice ,Prosencephalon ,S100 Calcium Binding Protein G ,Cell Movement ,Interneurons ,Cortex (anatomy) ,Neural Pathways ,medicine ,Animals ,education ,Cerebral Cortex ,Mice, Inbred ICR ,education.field_of_study ,Cerebrum ,General Neuroscience ,Anatomy ,Embryo, Mammalian ,Transplantation ,Electroporation ,medicine.anatomical_structure ,nervous system ,Forebrain ,Neuroscience - Abstract
The migratory paths of interneurons derived from the ganglionic eminence (GE), and particularly its caudal portion (CGE), remain essentially unknown. To clarify the three-dimensional migration profile of interneurons derived from each part of the GE, we developed a technique involving focal electroporation into a small, defined portion of the telencephalic hemisphere. While the medial GE cells migrated laterally and spread widely throughout the cortex, the majority of the CGE cells migrated caudally toward the caudal-most end of the telencephalon. Time-lapse imaging and anin vivoimmunohistochemical study confirmed the existence of a migratory stream depicted by a population of CGE cells directed caudally that eventually reached the hippocampus. Transplantation experiments suggested that the caudal direction of migration of the CGE cells was intrinsically determined as early as embryonic day 13.5. The caudal migratory stream is a novel migratory path for a population of CGE-derived interneurons passing from the subpallium to the hippocampus.
- Published
- 2005
22. A case of congenital solitary testicular myofibroma associated with an undescended testis
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Evelyn Ervine, Kiarash Taghavi, Philip Morreau, Masato Yozu, and Mike Watson
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Pathology ,medicine.medical_specialty ,Text mining ,business.industry ,Myofibroma ,Medicine ,business ,Pathology and Forensic Medicine - Published
- 2013
23. Birth-date dependent alignment of GABAergic neurons occurs in a different pattern from that of non-GABAergic neurons in the developing mouse visual cortex
- Author
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Masato Yozu, Kazunori Nakajima, and Hidenori Tabata
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Male ,Interneuron ,Cell Count ,Biology ,gamma-Aminobutyric acid ,Mice ,S100 Calcium Binding Protein G ,Cell Movement ,Interneurons ,Pregnancy ,Cortex (anatomy) ,Neural Pathways ,medicine ,Animals ,gamma-Aminobutyric Acid ,Visual Cortex ,Critical period ,Neurons ,Mice, Inbred ICR ,Critical Period, Psychological ,General Neuroscience ,General Medicine ,Embryo, Mammalian ,Immunohistochemistry ,Embryonic stem cell ,medicine.anatomical_structure ,Visual cortex ,Animals, Newborn ,Bromodeoxyuridine ,nervous system ,Calbindin 2 ,GABAergic ,Female ,Calretinin ,Somatostatin ,Neuroscience ,medicine.drug - Abstract
In the developing mouse cerebral cortex, gamma-aminobutyric acid (GABA)ergic neurons and non-GABAergic neurons arise in distinct places and migrate into the cortical plate (CP) via different pathways. Although the "inside-out" alignment of projection neurons in the cortex has been thoroughly analyzed, the pattern of interneuron alignment is not well understood. Herein, we show that in the postnatal day (P) 9.5 mouse visual cortex, GABAergic neurons born on embryonic day (E) 12.5 were distributed around two peak locations, mainly around layer V and also around layer II/III, while non-GABAergic neurons born on E12.5 were distributed around only one peak in layer VI. Both cell populations born on E15.5 exhibited only one common peak distribution in layer II/III. The two peak locations of GABAergic neurons born on E12.5 still existed at P30. When the subtypes of GABAergic neurons were analyzed, calretinin-positive cells born on E12.5 were distributed in the cortex around one peak location near layer II/III, whereas somatostatin-positive E12.5 cells were distributed in the cortex around one peak location near layer V. These results suggest that the alignment of interneurons is regulated differently according to subtypes and from that of projection neurons having the same embryonic day of origin.
- Published
- 2004
24. Cutaneous squamous cell carcinoma associated with proliferation of osteoclast-like giant cells
- Author
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Masato, Yozu, Joanna, Glengarry, and Syed Salahuddin, Ahmed
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Male ,Skin Neoplasms ,Antigens, CD ,Biomarkers, Tumor ,Carcinoma, Squamous Cell ,Antigens, Differentiation, Myelomonocytic ,Humans ,Keratins ,Osteoclasts ,Vimentin ,Giant Cells ,Aged ,Cell Proliferation - Abstract
Proliferation of osteoclast-like giant cells in a cutaneous squamous cell carcinoma is a rare phenomenon and so far only four cases have been reported. In previous reports, osteoclast-like giant cells were admixed with sarcomatoid component of squamous cell carcinoma and it is therefore debatable if the osteoclast-like giant cells represent a reactive phenomenon or a part of the malignant tumour. A case of cutaneous squamous cell carcinoma associated with osteoclast-like giant cells is reported. However, sarcomatous component of squamous cell carcinoma was not identified in this case. Morphologically, the osteloclast-like giant cells appeared to be benign. The localization of the squamous cell carcinoma and the osteoclastic-like giant cells were separate from one another. Immunohistochemically, squamous cell carcinoma was positive for high molecular weight cytokeratin, cytokeratin-5 and p63, whereas the osteloclast-like giant cells were positive for histiocyte marker CD68 and vimentin and negative for epithelial markers supporting a reactive nature of osteoclast-like giant cells to the cutaneous malignancy.
- Published
- 2012
25. Cell-autonomous roles of ARX in cell proliferation and neuronal migration during corticogenesis
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Jamel Chelly, Shigeaki Kanatani, Mary Antypa, John G. Parnavelas, Gaëlle Friocourt, Masato Yozu, Hidenori Tabata, Takao Takahashi, Kazunori Nakajima, Odile Raguenes, and Claude Férec
- Subjects
Doublecortin Protein ,Ganglionic eminence ,Interneuron ,Green Fluorescent Proteins ,Lissencephaly ,Mice, Transgenic ,Nerve Tissue Proteins ,Biology ,Cell fate determination ,Transfection ,Interneuron migration ,Rats, Sprague-Dawley ,Mice ,Cell Movement ,Chlorocebus aethiops ,medicine ,Animals ,Progenitor cell ,Cells, Cultured ,gamma-Aminobutyric Acid ,Cell Proliferation ,Cerebral Cortex ,Homeodomain Proteins ,Neurons ,Mice, Inbred ICR ,General Neuroscience ,Cell Differentiation ,Articles ,Cell cycle ,medicine.disease ,Embryo, Mammalian ,Rats ,Corticogenesis ,medicine.anatomical_structure ,Electroporation ,Ki-67 Antigen ,nervous system ,Bromodeoxyuridine ,Gene Expression Regulation ,RNA Interference ,Neuroscience ,Transcription Factors - Abstract
The aristaless-related homeobox (ARX) gene has been implicated in a wide spectrum of disorders ranging from phenotypes with severe neuronal migration defects, such as lissencephaly, to mild forms of X-linked mental retardation without apparent brain abnormalities. To better understand its role in corticogenesis, we usedin uteroelectroporation to knock down or overexpress ARX. We show here that targeted inhibition of ARX causes cortical progenitor cells to exit the cell cycle prematurely and impairs their migration toward the cortical plate. In contrast, ARX overexpression increases the length of the cell cycle. In addition, we report that RNA interference-mediated inactivation of ARX prevents cells from acquiring multipolar morphology in the subventricular and intermediate zones, resulting in decreased neuronal motility. In contrast, ARX overexpression appears to promote the development of tangentially oriented processes of cells in the subventricular and intermediate zones and affects radial migration of pyramidal neurons. We also demonstrate that the level of ARX expression is important for tangential migration of GABA-containing interneurons, because both inactivation and overexpression of the gene impair their migration from the ganglionic eminence. However, our data suggest that ARX is not directly involved in GABAergic cell fate specification. Overall, these results identify multiple and distinct cell-autonomous roles for ARX in corticogenesis.
- Published
- 2008
26. Migratory behavior of presumptive interneurons is affected by AMPA receptor activation in slice cultures of embryonic mouse neocortex
- Author
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Masato Yozu, Kazunori Nakajima, Hidenori Tabata, Norbert König, Gifu Academy of Forest Science and Culture, Laboratoire de neurogénétique, Université Montpellier 2 - Sciences et Techniques (UM2)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR122, School of Applied and Engineering physics [Ithaca] (AEP Cornell), Cornell University [New York], and Dept. of Electrical and Computer Engineering
- Subjects
MESH: Dose-Response Relationship, Drug ,Mice ,0302 clinical medicine ,Cell Movement ,MESH: Gene Expression Regulation, Developmental ,Excitatory Amino Acid Agonists ,MESH: Animals ,Receptor ,MESH: Cell Movement ,[SDV.BDD]Life Sciences [q-bio]/Development Biology ,Cerebral Cortex ,0303 health sciences ,Mice, Inbred ICR ,Neocortex ,MESH: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid ,musculoskeletal, neural, and ocular physiology ,Stem Cells ,Glutamate receptor ,Gene Expression Regulation, Developmental ,Cell Differentiation ,Transfection ,MESH: Interneurons ,medicine.anatomical_structure ,Neurology ,Cerebral cortex ,MESH: Receptors, AMPA ,Female ,MESH: Cell Differentiation ,Ganglionic eminence ,AMPA receptor ,MESH: Stem Cells ,Biology ,03 medical and health sciences ,Organ Culture Techniques ,Developmental Neuroscience ,Interneurons ,medicine ,Animals ,Cell Lineage ,Receptors, AMPA ,MESH: Mice, Inbred ICR ,MESH: Mice ,alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid ,030304 developmental biology ,Dose-Response Relationship, Drug ,MESH: Transfection ,MESH: Cell Lineage ,Embryonic stem cell ,MESH: Organ Culture Techniques ,MESH: Cerebral Cortex ,nervous system ,MESH: Excitatory Amino Acid Agonists ,Neuroscience ,MESH: Female ,030217 neurology & neurosurgery - Abstract
It has been reported that functional α-amino-3-hydroxy-5-methyl-isoxazolpro-prionic acid (AMPA) receptors permeable to calcium are already expressed by tangentially migrating prospective interneurons in the developing rodent cerebral cortex. However, the role of these receptors is not yet fully understood. To examine the effect of activation of AMPA receptors on tangential migration, we exposed migrating prospective interneurons derived from the medial ganglionic eminence (MGE) to AMPA in slice cultures and performed time lapse imaging. In the neocortex, a subpopulation of MGE-derived cells stopped migration or changed the direction of migration in response to AMPA in a dose-dependent manner. In contrast, neither MGE-derived cells migrating in the subcortical territory nor radially migrating cells in the neocortex were affected by exposure to AMPA. Transfection of dominant-negative AMPA receptor subunit GluR1 to the tangentially migrating cells prevented the effects of AMPA on migration. This study provides evidence that the activation of AMPA receptors can directly affect tangential migration in the neocortical part of telencephalic slice cultures.
- Published
- 2006
27. Immunohistochemical analysis for mismatch repair proteins on colorectal adenomas is a useful adjunctive study in identifying the muir-torre syndrome
- Author
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Masato Yozu, K.P. Wong, Jon A. Mathy, and Beryl Tan
- Subjects
Oncology ,medicine.medical_specialty ,Pathology ,High prevalence ,business.industry ,Cell ,medicine.disease ,Malignancy ,Pathology and Forensic Medicine ,medicine.anatomical_structure ,Muir–Torre syndrome ,Internal medicine ,medicine ,Clinicopathological features ,Immunohistochemistry ,DNA mismatch repair ,Basal cell ,business - Abstract
Background Identification of Muir-Torre syndrome (MTS) patients is crucial due to the significant impact on the clinical management. Aim The purpose of this study is to identify the high risk clini-copathological features of MTS including the analysis of immu-nohistochemical profile of mismatch repair (MMR) proteins on colorectal adenomas. Methods All of 14 patients who presented with sebaceous neopla-sia to our institution between 2002 and 2011, including 3 MTS and 11 non-MTS patients were examined. Results The high risk clinicopathological features of the MTS were: (1) presence of visceral malignancy (p = 0.0027), (2) high prevalence of epidermal malignancies (squamous cell carcinomas and basal cell carcinomas) (p Discussion The results suggest that immunohistochemistry for MMR proteins on colorectal adenomas can be a useful adjunctive study in identifying MTS.
- Published
- 2013
28. Muir–torre syndrome-associated pleomorphic liposarcoma arising in a previous radiation field
- Author
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Daniel Ng, Michael Dray, Jennifer Griffin, K.P. Wong, Pennie J. Symmans, Masato Yozu, Catherine H. Han, and Susan Parry
- Subjects
Male ,congenital, hereditary, and neonatal diseases and abnormalities ,Pathology ,medicine.medical_specialty ,Neoplasms, Radiation-Induced ,Biology ,MLH1 ,Pleomorphic Liposarcoma ,Pathology and Forensic Medicine ,Germline mutation ,Muir–Torre syndrome ,medicine ,Humans ,Molecular Biology ,neoplasms ,In Situ Hybridization, Fluorescence ,Aged ,nutritional and metabolic diseases ,Cell Biology ,General Medicine ,Liposarcoma ,medicine.disease ,Immunohistochemistry ,digestive system diseases ,Lynch syndrome ,DNA-Binding Proteins ,MSH6 ,MutS Homolog 2 Protein ,Muir-Torre Syndrome ,MSH2 ,Sarcoma - Abstract
Background Muir–Torre syndrome is a variant of Lynch syndrome, characterised by sebaceous neoplasia and/or keratoacan-thomas associated with visceral malignancies. Muir–Torre syndrome is caused by germline mutations of one of the mismatch repair genes, frequently MSH2 and less frequently MLH1 and MSH6. Visceral malignancies associated with Muir–Torre syndrome and Lynch syndrome include colorectal, endometrial and other gastrointestinal, urological and gynaecological malignancies. Small numbers of Lynch syndrome-associated soft tissue sarcomas have been reported but there are no reported cases of soft tissue sarcomas in Muir–Torre syndrome. Aim and Methods In this study, we report a 74-year-old man with known Muir–Torre syndrome with confirmed MSH2 germ-line mutation, diagnosed with pleomorphic liposarcoma of the right buttock in a previous radiation field. The tumour showed loss of expression of MSH2 and MSH6 on immunohistochemistry. Results Immunohistochemistry on another pleomorphic liposar-coma in a different patient with no previous history of Muir–Torre syndrome or Lynch syndrome showed no loss of expression of mismatch repair proteins. Discussion This is the first report of Muir–Torre syndrome-associated sarcoma and the first case of post-radiation sarcoma in Lynch syndrome.
- Published
- 2013
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